Week 7: Circulation and Tissue Perfusion Flashcards
Interconnected Systems of the Heart
- Structures
- Electrophysiology – electrical conduction to create heartbeat
- Vasculature – blood supply to heart muscle itself
Perfusion
flow of blood through circulatory system to oxygenate cells and remove rate
Poor perfusion results in cell death over time
Perfusion depends on:
Sufficient cardiac output
Sufficient blood pressure
Cardiac Output
amount of blood the heart is pumping
- Heart rate x stroke volume
- Normal = 75 x 70 = 5250ml/min
- Heart rate – electrical activity that pumps the heart
- Stroke volume – volume of blood in the heart when it pumps
Influenced by:
o Nervous systems
o Fluid volume
o Heart muscle contraction
o Resistance in vessels (peripheral resistance) – resistance of the arteries to blood
flow
Blood Pressure
Cardiac output x peripheral resistance
Influenced by:
o Heart rate (contractility)
o Stoke volume (fluid, contraction, return, constriction)
o Blood viscosity
o Radius of vessel (constriction, atherosclerosis, blood volume)
P wave
activation of atria
QRS complex
activation of ventricles
T wave
recovery wave
Primary Causes of Problems with Perfusion
- Vascular volume disorders – FVO, FVD
- Electrical disorders – dysrhythmias
- Mechanical disorders – cardiac myopathy, CHF
- Coagulation disorders – blood clots (can lead to MI)
Modifiable risk factors for CV disease (co-morbidities)
HTN - damage to vessels over time
Obesity – increased demand on all body systems
Dyslipidemia – buildup blocks vessels and impacts flow
Diabetes – damage to vessels over time
Lifestyle – diet, exercise, smoking, alcohol
Sleep apnea – hypoxia (comp. causes damage)
Smoking – increase plaque formation
Non-modifiable risk factors: Cardiac /CV disease
Family history – increased risk for diagnosis in immediate family
Genetics – may modify cholesterol, heart structure, etc.
Gender – men more predisposed to CVD, women more predisposed to
stroke
Cardiac Physical exam RED flags
Changes in VS – compensation
Altered breath sounds – impaired movement through pulmonary vessels (CHF)
Restlessness, changing LOC – brain hypoxia
Changes in cardiac assessment – structures, electrophysiology,
vasculature
Fatigue – body systems not functioning
SOB – compensation for decreased oxygenation to body
Pain – tissue hypoxia (squeezing/racing palpations, SOB, nausea,
shoulder/jaw pain, anxiety, impending doom, fatigue, dizziness)
ACE Inhibitors
blocks the release of ACE, stopping the RAAS system, decreasing blood
pressure
ARBs
blocks the binding of Angiotensin II (RAAS system), stopping the vasoconstriction
of vessels, decreasing blood pressure
Beta blockers
blocks beta receptors (epinephrine + norepinephrine) binding,
decreasing contraction and heart rate
Calcium channel blockers
blocks calcium channels, stopping calcium from entering the
heart, decreasing contraction and heart rate
Hypertension
chronic condition where BP remains consistently elevated above set range
Causes stress to body systems, which causes damage
Compensation may occur in an attempt to lower blood pressure - chronic compensation
when body is unsuccessful in reducing BP, causes damage
Major risk factor for heart attack and stroke
Categories of Hypertension
Patients without diabetes = +140/90
Patients with diabetes = +130/80 (comorbidity, body can handle less
Primary Hypertension
No cause, 95%
Secondary Hypertension
Identifiable cause, 5%
Causes: CKD, sleep apnea, pregnancy, NSAID use, alcoholism
Non-modifiable risk factors: Hypertension
Family history
55+ men, 65+ women
Men are at higher risk
Genetics
SDOHs
Modifiable risk factors: hypertension
Lifestyle – activity & diet (sedentary, sodium)
Alcohol
Smoking
Weight
Physical exam: hypertension
Vitals – BP
Cardiac exam
Systems assessment for symptoms of HTN – Silent Killer (often asymptomatic!)
- Headache
- SOB
- Visual disturbances
- Chest pain
- Irregular rhythm
- Bounding pulse
- Nausea/vomiting
Nursing Priorities for Hypertension
Monitor patterns
Diagnosis requires elevation over time
Response to treatment/lifestyle changes
- Intake/Output
Interaction between BP and fluid balance
Lifestyle: hypertension
Reduce risk
Eat – lots of fruits, vegetables, low-fat dairy products, low saturated fats
(DASH DIET)
Quit – smoking
Moderate – alcohol
Reduce - sodium intake, stress
Maintain – health body weight
Increase – exercise (at least 30min/day)
Pharmacological Interventions for Hypertension
ACE inhibitors
ARBs
Beta-blockers
Calcium channel blockers Diuretics
Hydralazine (vasodilator)
targets of therapy: hypertension
Lower peripheral resistance
Lower cardiac output
Reduce RAAS system & fluid volume
Why Treatment is not Working to Improve BP:
- Adherence
- Unidentified/untreated associated condition (sleep apnea, alcoholism, pain, etc.)
- Drug interactions (OTC supplements, NSAIDs, oral contraceptives)
- White Coat HTN
- Inappropriate treatment regimen
Hypertensive crisis
BP = +180/120
- Acute marked increase in BP
- Emergency or urgent
Signs & symptoms:
Chest pain
SOB
Back pain
Visual disturbances
Cerebral edema
Headache
Urgent:
Headache
Nosebleeds
Anxiety
hypertensive crisis: pharmacological treatment
Emergency – IV vasodilator
Urgent – fast acting oral antihypertensive
Treating a Hypertensive Crisis
Notify provider
- Assessment:
VS monitoring (q 5mins)
Systems assessment (organ damage)
Blood work:
Urinalysis
Electrolytes (K, Mg, Cl, Na)
Kidney markers
Lipids
Blood sugars
12 lead ECG
Intake/Output tracking
Patient education:
Bedrest
Notify of change in symptoms
Reduce stimuli
Nurse Management of Hypertensive Crisis
- Administer O2 (allows for perfusion)
- Monitor BP frequently
- Monitor cardiac, respiratory, and neuro frequently
- Initiate IV access
- Administer meds – IV antihypertensive
- Assess cardiac monitor
- Encourage bedrest and reduce stimuli
Atrial Fibrillation (AFIB)
irregular & often rapid heart rhythm caused by uncoordinated contraction of atrial muscles
Arrhythmia/dysrhythmia
- Significant increase in mortality
Normal – atria fire synchronously to pump blood into ventricles
A Fib – rapid, chaotic, and irregular contraction pattern of atria; caused by
electrophysiological or structural changes of the atria tissues
ECG of A Fib
Rate – usually over 100
Rhythm – irregular
P wave – non-existent
PR interval – impossible to compute
QRS complex – normal (ventricles, not atria, remains normal)
Causes of A Fib
HTN – chronic activation of compensation mechanisms causes structural and
electrophysiological changes
Diabetes – vascular changes
Smoking – nicotine causes inflammation & oxidative stress
Obesity – weight-related changes to structure
Alcohol – triggers arrhythmias
Outcomes of A Fib
Rapid firing of atria – blood pooling, clot formation
o TIAs
o Ischemic stroke
o MI
o Pulmonaryembolism o Heartfailure
- Also causes poor pumping, lower CO, poor perfusion
Health History: A Fib
Non-modifiable risks:
o Family history
o Age
o Gender
o Genetics
o SDOH
- Modifiable risks:
o Lifestyle: activity (sedentary) diet, (sodium)
o Alcohol consumption
o Smoking
o Weight - Other relevant data:
o Comorbidities – HTN, hyperthyroidism, hypokalemia, hypomagnesia
o Signs & symptoms
Physical Assessment: A Fib
- SOB
- Exertion fatigue
- Irregular, increased HR
- Weak pulse
- Palpations
- Hypotension
- Abnormal heart sounds
- Chest pain
Nursing Priorities: A Fib
- Decrease risk of emboli – anticoagulation therapy
- Rhythm control – manage arrythmia through medication
- Health teaching – treatment/lifestyle modifications, health literacy, readiness for
change, support system
Pharmacological Intervention: A Fib
Target – decrease HR, regulate rhythm, promote clot prevention
Types:
Calcium channel blockers
Beta-blockers
Cardiac glycoside (Digoxin)
Oral anticoagulants
Acute Intervention: A Fib
- Transesophageal Echocardiogram (TEE)
- Synchronized Cardioversion
- Catheter ablation – tissue with irregular pulse is damaged
