LO1 Cardiovascular Disorders Flashcards
Deep Vein Thrombosis (DVT)
A thrombosis is a blood clot that remains attached to a vessel wall.
what is the cause of Deep Vein Thrombosis (DVT)
Intimal irritation, roughening, inflammation, traumatic injury, infection, low blood pressures, or obstructions that cause blood stasis
Inflammation is the usual cause of DVT
causes of DVT
History of trauma Sepsis Stasis or inactivity Recent immobilization Pregnancy Birth control pills Malignancy Coagulopathies Smoking Varicose veins
signs and symptoms of DVT
Pain Edema Increase temp extremity Erythema Tenderness
Atherosclerosis
Fatty build up
Affects the inner lining of the aorta, cerebral, and coronary blood vessels.
Abnormal thickening and hardening of vessel walls
what is Atherosclerosis caused by
Caused by soft deposits of intra-arterial fat and fibrin which harden over time
Risk Factors for atherosclerosis
Hypertension (HTN)
Cigarette smoking: thickens vessel walls making it hard for blood to pass through
Diabetes
High serum cholesterol levels
Lack of exercise
Obesity
Family history of heart disease or stroke
Male sex
Effects of Arteriosclerosis
loss of elasticity in vessel walls
Partial obstruction of vessel lumen (Ischemia)
Complete obstruction of vessel lumen (Infarction, Necrosis)
Thrombosis
Embolism (Obstruction,
Infarction (Heart and Brain)
—Infarction: complete obstruction
Aneurysm (Rupture, Exsanguination)
Vessel calcification (Rigidity, Rupture)
Aneurysm
“dilation of a vessel”
Artery wall weakness
most common cause for AAA
Atherosclerosis
Signs and Symptoms of a ruptured aneurysm
Shock
Pain, usually describe as sharp stabbing in nature.
Back pain
Difference in blood pressure
between arms
Absent radial or femoral pulse
Mottling of extremities below
aneurysm
modeling: spider veins, bluish white skin
absent radial or femoral pulses
Hypertension
Known as lanthanic (silent) disease
Characterized by a consistent elevation of systemic arterial blood pressure
Often defined by a resting BP consistently greater than 140/90 mm Hg
Risk Factors of hypertension
Family history
Advancing age
Gender (men younger than 55, women older than 74): structural changes of vessels
Black race: social status
High dietary sodium intake
Glucose intolerance: higher cholesterol
Cigarette smoking
Obesity
Heavy alcohol consumption
Low dietary intake of potassium, calcium and magnesium
Pathophysiology of hypertension
Damages walls of systemic blood vessels
Prolonged vasoconstriction and high pressures with in the arteries and arterioles stimulate the vessels to thicken and strengthen
End result is a permanently narrowed blood vessel
Treatment Plans
Arteriosclerosis Peripheral Vascular Disease Hypertension Deep Vein Thrombosis Aneurysm
*symptomatic only
Endocarditis
Inflammation of the inner lining of the heart, and/or heart valves
causes of endocarditis
Can be caused by either bacteria or virus, bacteria being the most common
risk factors of endocarditis
Acquired valvular heart disease (mitral valve prolapse)
Implantation of prosthetic heart valves
Congenital lesions
Previous attack
Male gender
Intravenous drug use: dirty needles
Long term indwelling catheterization
Signs and Symptoms of endocarditis
May involve a number of organ systems
Classic findings
Fever
Cardiac murmur
Petechial lesions of skin, conjunctiva, and oral mucosa
Chest pain- SOB
myocarditis
Is an inflammation of the heart muscle (myocardium)
Results from infection (bacteria or viral) or toxic inflammation (drugs or toxins from infectious agents)
Cocaine users are 5x more likely to get it
myocarditis causes
Chest infection
Auto immune disease
Fungal viral infection
signs and symptoms of myocarditis
Flulike
Pain in epigastric region or under sternum (substernal)
Dyspnea
Cardiac arrhythmias
Stabbing chest pain
pericarditis
Inflammation of the pericardium, two thin layers of a sac-like tissue surround the heart, hold it in place and help it work.
Normally, a small amount of fluid keeps the layers separate so that there’s no friction between them.
Signs and Symptoms Pericarditis
Low cardiac output
Low SPO2
Chest pain
causes of pericarditis
Trauma
Heart attacks
Acute Coronary Syndrome (ACS)
refers to distinct conditions caused by a similar sequence of pathologic events involving abruptly reduced coronary blood flow
Acute Coronary Syndrome (ACS) conditions
Unstable Angina (UA
Non-ST-segment elevation myocardial infarction (NSTEMI),
ST-segment elevation myocardial infarction (STEMI)
Ischemia
Lack of oxygen to the tissues
ST depression or T inversion
Ischemic Heart Disease
Myocardial ischemia is usually the route of the blockage or gradual narrowing of one or more of the coronary arteries by atheromatous plaque.
Narrowing or blockage of a coronary artery can disrupt the oxygen supply to the area of the heart supplied by the affected vessel.
If the cause of the ischemia is not reversed and blood flow restored to the affected area of the heart muscle, ischemia may lead to cellular injury and ultimately, cellular death
Clinical Features of Ischemic Heart Disease
retrosternal chest pain, pressure, heaviness squeezing lasting 10 minutes or longer that usually occurs at rest or with minimal exertion
Can be accompanied by angina equivalents such as unexplained new-onset or increased exertional dyspnea, unexplained fatigue, diaphoresis, nausea/vomiting, or syncope
atypical presentation of Ischemic Heart Disease
may include pleuritic chest pain, epigastric pain, acute-onset indigestion, or increasing dyspnea without chest pain.
Atypical presentations are most often observed in younger(25 to 40 years of age) and older(over 75 years) patients, women, and patients with Diabetes Mellitus, chronic renal insufficiency, or dementia
what does schema lead to
Injury
prolonged ischemia
ST elevation
infarct
death of tissue
may or may not show in Q wave
angina Three types:
Stable Angina (Exertional Angina)
Unstable Angina (Preinfarction Angina)
Prinzmetal’s Angina
Prinzmetal’s Angina
Vasospastic angina: no blockage or clot just spasm of segment of coronary artery
Cause: cocaine
Treatment: nitro
Angina
Imbalance between myocardial O2 supply and demand
choking pain in the chest” Burning Tightness Pressure Crushing heavy
The coronary arteries can spasm as a result of :
Exposure to cold weather Stress Medicines- Anti-migraines, Chemo, Antibiotics Smoking Cocaine use
Myocardial Infarction
Sudden and total occlusion or near‐ occlusion of blood flowing through an affected coronary artery to an area of heart muscle
Results in ischemia, injury, and necrosis of the area of myocardium distal to the occlusion.
If blood flow is not restored to the affected artery
myocardial cells within the sub-endocardial area begin signs of injury within 20 to 40 minutes.
ACS Management/ Treatment
Reduce physical activity, calm reassurance
O2 if WOB increased and SPO2 less than 94%, if pale, if SOB
If clinically indicated ASA 160-325mg PO
–81mg X2= 162mg
3 Lead followed by 12 Lead ECG noted
IV BEEFORE NITRO
- -0.4mg spray
- -1 every 3-5 mins
- -At 3 min mark vitals and re assess
If clinically indicated, Nitro 0.4mg SL, titrate to effect
Consider calling ALS
Notify receiving hospital if ST elevation
ACS CALL vs NON ACS CALL
ACS CALL
Heavy, burning tight
NON ACS CALL
Sharp pain
Increases with palpation
Increase with inspiration
angina signs and symptoms
“choking pain in the chest”
Burning
Tightness
Pressure
Crushing
Heavy
Radiates
Lasts less than 20 min
Sob
Occurs with activity
Is better with rest
UNSTABLE angina signs and symptoms
Lasts longer than 20mins
Can occur at rest
MI: STEMI, NSTEMI signs and symptoms
At rest
Doesn’t get better
Shock symptoms
- -Nausea vomiting
- -Pale cool clammy
Cardiomyopathies
Diverse group of diseases that affect the myocardium
Most result from underlying disorders
In response to injury, the heart may undergo dilation or hypertrophy
Cardiomyopathies are incurable diseases and the only hope is heart transplantation
Cardiomyopathies are divided into three forms:
Dilated Cardiomyopathy
Hypertrophic cardiomyopathy
Restrictive cardiomyopathy
cardiac output
stroke volume
Formula
Cardiac output (CO): amount of blood ejected by each ventricle in 1 minute
Stroke volume (SV): amount of blood pumped by each ventricle in 1 beat (mL/beat)
CO=SV X HR
70ml/beat x 75 bpm+ 5250mL/min
Factors that affect CO
- Heart rate
- Preload:
- afterload:
- Contractility:
define preload and after load
Preload: amount of blood entering ventricles @ diastole (rest) à nitro decreases preload
afterload: resistance ventricles have to overcome to circulate blood à decreasing afterload decreases back up into the lungs
Pulmonary Edema
Swelling within the lungs
Sign of left sided CHF
Decrease of output to left side of heart
One of the most common causes of pulmonary oedema is
left ventricular failure from an acute MI
Other cause are inhaled toxins, infections, and sometimes trauma and altitude changes
Pulmonary Edema Signs and Symptoms
In early pulmonary edema you will hear late inspiratory crackles at the lung apices.
These crackles are caused by rapid expansion of collapsed alveoli as they reach maximum inflation
As pulmonary edema worsens you will hear more proximal crackles in lung fields
As fluid migrates into larger more central airways and mix with mucus the crackles become more coarse sounding.
As lungs fill up frothy pink sputum may appear, which an ominous sign.
Happens acutely
Congestive Heart Failure
heart failure may present acutely as a result of acute pump dysfunction from an mi
Heart is unable to pump powerfully enough or fast enough to empty its chambers.
Blood backs up into the systemic circuit, the pulmonary circuit, or both.
Left sided CHF
Pumps blood to body
Pulmonary hypertension
Back up into the lungs
Crackles in lungs
SOB
Left sided heart failure is most commonly caused by an AMI and chronically by continued hypertension.
Left-sided heart failure signs and symptoms
Extreme restlessness and anxiety, confusion and agitation
Severe dyspnea, tachypnea, tachycardia
Hypertension or hypotension
Crackles and/or wheezes
Frothy pink sputum in severe cases
Right sided CHF
Pumps blood to lungs
JVD
Pedal edema
Pitting edema
SOB
Right-Sided heart failure Signs and Symptoms
Jugular vein distention
Pedal/pitting edema
Heart Failure Management
Position of comfort, most often high fowlers
If clinically indicated administer nebulized sympathomimetic/anti-cholinergic
If clinically indicated initiate Continuous Positive Airway Pressure (CPAP)
Consider ALS intercept
If clinically indicated administer SL nitroglycerine
Pulmonary edema treatment
Crackles: nitro
CPAP
Wheezing: Ventolin and Atrovent
–Call ALS if Combivent doesn’t work
Nitro for pulmonary edema
No chest pain and no nitro prescription –> call med control for orders
No chest pain- nitro prescription –>give nitro
Chest pain –> give nitro
Causes for pulmonary edema
Cardiogenic
Noncardiogenic
Cardiogenic
Noncardiogenic
Cardiogenic
- Left sided failure
- Systemic hypertension
Noncardiogenic
- Toxins
- Lung infections
- Sepsis
Pneumonia Vs Pulmonary Edema
–Pulmonary edema: cause by Left heart failure
Normal HR
Febrile
course Crackles
Wheeze
May or may not be productive cough- punk or white
History of CHF
Cardiac CP- won’t increase with inspiration
---Pneumonia: infection Fast HR Fever thick Crackles Wheeze Productive cough- green or dark yellow History of pneumpnia Sharp CP Cp increase with inspiration/coughing
Cardiogenic Shock
Heart is so severely damaged that it can no longer pump a volume of blood sufficient to maintain tissue perfusion.
When 25% of the left ventricular myocardium is involved
When 40% or more of the left ventricle has been infarcted (tissue death)
High mortality rate
Signs and symptoms of cardiogenic shock
brain
Altered LOC
Coma
Lethargy
Possible stroke
Signs and symptoms of cardiogenic shock
lungs
SOB
Accessory muscle use
Stats less than 90
Tachnyepia
Signs and symptoms of cardiogenic shock
heart
Increase HR
Decrease BP
Arythmias
MI
Signs and symptoms of cardiogenic shock
skin
Cool
Clammy
Delayed cap refill
Management of Cardiogenic Shock
Focuses on improving oxygenation and peripheral perfusion
Secure the airway and administer 100% supplemental oxygen.
Advanced airway necessary if the patient is comatose.
Place the patient in a supine position.
IV with normal saline
Frank-starling mechanism
One characteristic of cardiac muscle is that when it’s stretched a contract with greater force
systematic vascular resistance leads to
a higher after load in the cardiac output can drop or heart rate has to work harder to maintain the same cardiac output which increases oxygen demand
- Changes in contractility may be induced by
medication’s that have a positive or negative inotropic effect
- Nervous system controls regulate the
contractility of the heart from beat to beat
- Positive chronotropic effect
how hard can increase its cardio output by increasing the number of contractions per minute (HR)
- Pacemaker
the area of conduction tissue in which the electrical activity arises at any given time
- AV node
is gatekeeper to the ventricles
o In 85-90% of humans blood supply comes from the branch of the RCA
o 10-15% of ppl it comes from the left circumflex artery
- Electric impulses from SA node take how may secs to read AV node
o.o8secs
- The conduction is delayed in the AV node for approximately how many secs
0.12sec
- It takes approx. how many sec for an electrical impulse to spread across the ventricles
0.08
what happens with ions during depolarization
depolarization sodium and calcium ions rush into cell causing inside of cell to be positive
what happens with ions during repolarization
the sodium and calcium channels close and potassium channels open allowing rapid escape of potassium ions from the cell
- Refectory period
period when the cell is depolarized or in the process of repolarizing
- Absolute refractory period
the cell is still highly depolarized and a new action protentional cannot be initialed
- Relative refractory period
the heart is partially depolarized and a new action potential will be inhibited but not impossible
The parasympathetic nervous system
- Sends messages mainly through vagus nerve
- Atropine blocks actions of PNS and vagus nerve causing HR to increase
The sympathetic nervous system
- Release norepinephrine ttavels to SA node, AV node and ventricles
- every beta agents effects the heart by increases hearts rate, force and automaticity
- Vasoconstriction is cause by alpha agent
- Vasodilation is caused by beta agent
- Alpha 1 receptors
are primarily located on peripheral blood vessels and stimulation results in: o Peripheral vasoconstriction o Mild bronchoconstriction o Increased metabolism o Stimulation of sweat glands
- Alpha 2 receptors
are primarily located on nerve endings and stimulation results in:
o Control release of neurotransmitters
- Beta 1 receptors
are primarily located within the cardiovascular system and stimulation results in:
o Increased heart rate (positive chronotropic)
o Increased strength of cardiac contraction (positive inotropic)
o Increased cardiac conduction (positive dromotropic)
- Beta 2 receptors
are primarily located on bronchial smooth muscle and stimulation results in:
o Bronchodilation
o Peripheral vasodilation
Causes of dysrhythmias
- Acid base disturbance
- ANS imbalance
- CNS damage
- Certain poisons
- Drugs
- Endocrine disorders
- Hypothermia
- Hypoxemia
- Ischemia o infarction
- trauma
- disrhythmias happen after an AMI for 2 reasons
- irritability of the ischemic heart muscle surrounding the infarct may cause the damage muscle to generate abnormal cardiac contractions
- because the infarct damages the conduction
