Cardiovascular Flashcards
Cardiac output (CO)
Stroke volume (SV) x Heart rate (HR)
Normal CO: 4 to 6 L/minute in adults
Stroke volume
The amount of blood pumped out of the left ventricle into the aorta in one minute.
Normal blood volume in adult body: 5 to 6 L
How do you increase cardiac output?
Increase stroke volume or increase heart rate - or both!
Preload
Pre-contraction workload (mm Hg). The volume of blood that fills ventricles (right side). Determined by venous return and the stretch of cardiac muscle fiber.
Afterload
Post-contraction workload (mm Hg). The pressure required to move blood into the aorta.
Systemic arterial pressure: Left side of the heart
Pulmonary arterial pressure: Right side of the heart
Frank Starling Law
“Volume of blood ejected by the ventricle depends on the volume present in the ventricle at the end of diastole”
SV and CO correlate directly with end-diastolic volume. As the heart fills up with more blood during diastole, it contracts harder and pumps out more blood during systole.
Matches output of right and left ventricles. Increased diastolic filling –> increase EDP –> increased myocardial fiber stretching –> increased CO
According to the Frank Starling Law, cardiac contractility is dependent on
Preload (volume)
Atherosclerosis etiology, risk factors, and causes
Etiology: Hardening of arteries due to fibrofatty lesions in the intimal lining; hypercholesterolemia
Risk factors: Family history of heart disease, gender/sex, old age, smoking, sedentary lifestyle
Causes: Peripheral artery disease, coronary artery disease, ischemic stroke
Clinical manifestations of atherosclerosis
Mild (asymptomatic): Hypertension
Severe (depends on vessel involved): Chest pain, dysrhythmias, neurological deficits, oliguria, protein cholesterol (HDL good, LDL bad), increased BUN/creatinine
Atherosclerosis plan, interventions, and evaluation
Plan: Correct underlying causes
Interventions: Smoking cessation, weight control, healthy diet (decreased fat intake), HMG-CoA reductase (decreased serum cholesterol), antiplatelet agents, surgical grafts/stents
Evaluation: Serum cholesterol levels within normal limits
Acute arterial occlusion etiology
Thrombus attached to vessel wall obstructs blood flow and pulses are absent below the occlusion. Freely moving emboli may be dislodged from the atrium and travel to smaller vessels causing atrial flutter and atrial fibrillation.
Acute arterial occlusion clinical manifestations
Extremities show the 7 Ps: Pistol shot, pallor, polar (cold), pulselessness, pain, paresthesia, paralysis. Cyanosis/mottling.
Acute arterial occlusion diagnosis and plan
Diagnosis: Medical history and assessment, radiography
Plan: Restore blood flow
Acute arterial occlusion sources
Freely moving emboli that travel to small vessels; cardiac valve surface emboli come from prosthetic cardiac valves (bacteria vegetation), fat emboli come from fractured bones/ortho surgery (look for petechiae), air emboli caused by lungs and IV lines, amniotic fluid emboli from childbirth.
Acute arterial occlusion interventions and evaluation
Interventions: Thrombolytic therapy, anticoagulant therapy (heparin), protect involved extremities from further injuries, embolectomy, amputation
Evaluation: Palpable distal pulses
Peripheral artery disease etiology and risk factors
Etiology: Atherosclerosis; symptoms of occluded arteries is subtle (femoral and popliteal arteries)
Risk factors: Older age, hypertension, cigarette smoking, diabetes mellitus
Peripheral artery disease clinical manifestations
Asymptomatic in less than 50% of occlusion. Weak pulses or loss of pulses below occlusion (pallor/polar), intermittent claudication (pain with walking), numbness, muscular atrophy, skin thin and shiny, brittle toenails, skin color pallor with elevation but red in dependent position, hair absent, lesions with gangrene, ulcers in toe tips, heels and lateral ankle, <5-15 sec capillary refill.
Peripheral artery disease diagnosis and plan
Diagnosis: Medical history and assessment, doppler, ultrasound, contrast resonance imaging (MRI)
Plan: Correct underlying issues
Peripheral artery disease interventions and evaluation
Interventions: Smoking cessation, protect affected tissue, ambulation, statins (decreases cholesterol), antiplatelet agents, vascular surgery, amputation
Evaluation: Palpable distal pulses, prosthetic placement
Venous thrombosis etiology and risk factors
Etiology: Presence of thrombus and intravascular inflammatory response
Risk factors: Inherited factor V deficiency, immobilization (increased DVT), orthopedic surgeries (joint replacement), oral contraceptives, increased blood viscosity (thickening) from airplane travel, prolonged sitting, and dehydration
Venous thrombosis clinical manifestations
Asymptomatic (partial occlusion), pulses present/weak, fever, malaise, lower extremities have pain/tenderness/swelling/dependent purplish color, flaky/thick/hardened skin (brown and blotchy), venous stasis ulcers in medial ankle or lower leg, >2 sec capillary refill, edema present, hair present/absent
Venous thrombosis diagnosis and plan
Diagnosis: Venography, ultrasonography, increased plasma D-dimer (>250 ng/mL), increased WBC, increased erythrocyte sedimentation rate
Plan: Prevent Virchow’s Triad (venous blood stasis, hypercoagulation, vessel wall injury)
Venous thrombosis interventions and evaluation
Interventions: Prevention; early ambulation post-surgery, avoid hip and knee flexion positions, HOB <30 degrees, apply heat to relieve venous spasms (NO MASSAGE), sequential compression devices for bedrest clients (prevention only-not for DVT), properly fitted anti-embolus stockings, anticoagulant therapy (heparin, warfarin, lovenox)
Evaluation: Pain free
During the initial admission assessment, the nurse documented abnormal lower extremity findings. Which finding reflects venous thrombosis?
Flaky skin, deep calf tenderness, and dependent purple color
Systolic BP
Peak pressure produced; ventricles contract.
S1 “lub” (mitral and tricuspid valves close)
Diastolic BP
Arterial pressure; ventricles are relaxed and filling.
S2 “dub” (aortic and pulmonic valves close); coronary arteries fill and oxygenate the myocardium
Pulse pressure
Force generated during systole creates pulse pressure.
Systole - Diastole = Pulse Pressure
Narrow pulse pressure
Hypovolemic shock (uncompensated BP drop); decreased stroke volume, increased heart rate
Wide pulse pressure
Increased intracranial pressure (head trauma), Cushing’s Triad (increased BP, bradycardia, irregular breathing), narrowed arterial lumens from increased systemic vascular resistance
Primary hypertension etiology and risk factors
Etiology: Idiopathic (insidious onset)
Risk factors: Age, race (prevalent in African Americans), heredity, smoking, excess ETOH, heavy salt diet, type 2 diabetes, dyslipidemia, cocaine
Secondary hypertension etiology
Adrenal cortical disorder (retention of water and salt), renal disease (atherosclerosis of the proximal renal artery/fibromuscular dysplasia), type 2 diabetes, oral contraceptives