Exam 3: Cardiovascular Disorders Flashcards
Shock
- Hypoperfusion, hypotension
- Failure of CV system to perfuse organs & tissues
- Not enough oxygenated blood goes to the body
Complications:
Acute respiratory distress syndrome
Acute renal failure
GI ischemia or poor motility due to redistribution of blood flow
Disseminated Intravascular Coagulopathy (DIC) - Immune activation of the clotting cascade
Multiple organ dysfunction syndrome (MODS)
Failure of two or more organ systems
Cardiogenic:
when the heart fails to pump blood sufficiently frequently seen with an MI, dysthymias, cardiac surgery
Hypovolemic shock:
diminished blood volume cases inadequate filling of vascular compartment causes can be hemorrhagic blood loss, severe dehydration, or with burn survivors
Obstructive shock:
an obstruction of the flow of blood through great veins, heart of lungs causes are dissecting aortic aneurysm, cardiac tamponade, most common is PE
Anaphylactic shock:
severe allergic reaction that cause vasodilation and increase capillary permeability. Generally due to drug or food reactions
Neurogenic shock:
Due to the loss of sympathetic nervous system generally with a person after a spinal cord injury at T6 and above
Septic shock:
severe infection activates the system inflammatory response with hypotension despite fluid resuscitation
Acute Coronary Syndrome (MI)
Etiology: Atherosclerosis, metabolic syndrome (3 or more of below)
Epidemiology: HTN, DM, HL, obesity, smoking, low HDL/high LDL, high triglycerides
Pathophysiology
Disease Process: Ischemic cardiac muscle from CAD -> could come from Thrombus, atherosclerosis, coronary vasospasm, anemia (least common). Ischemia occurs when coronary arteries are unable to dilate for increased needs.
Stable angina
CP goes away w/rest
Unstable angina
CP at rest
Clinical and electrocardiographic (ECG) findings without an elevated biomarker level (troponin).
Non-ST-segment elevation myocardial infarction (NSTEMI)
Troponin elevation and ECG changes, but no ST elevation
ST-segment elevation myocardial infarction (STEMI)
Troponin elevation and ST segment elevation
Arterial Diseases
Etiology: Endothelial dysfunction (?)
Epidemiology: Age, males, DM, HTN, smoking, HL, obesity, inactivity, chronic inflammation
Diagnosis: Pulse checks, Cap Refill, hx of CV disorder, ABI less than 1, labs, US, angiography, MRA, cardiac cath, angiogram, CT, ECG, stress testing, lipid panels
Prognosis/general statistics: limit S/S w/ pharm treatment and lifestyle changes. Surgical interventions (stent or graft)
Peripheral arterial disease
Atherosclerosis is most common cause. Decreased flow to peripheral arteries. Intermittent claudication.
Impacted limb 5 P’s: pain, pallor, paresthesia, palpable cool, perfusion reduction
Aneurysm
Damage to arterial lining usually r/t atherosclerosis, genetic disposition, vascular disease or trauma -> weakens wall and causes bulge or dilation. AAA most common. No symptoms until rupture. Creates turbulence (thrombus, dissection risk)
Raynaud’s Syndrome
Exaggerated sympathetic reflex -> vasoconstriction. Endothelial dysfunction (deficient NO and elevated vasoconstrictors). Increased platelet aggregation.
Dyslipidemia
Imbalance of lipid components - LDL (bad) and HDL (good)
hyperlipidemia
Atherosclerosis -
LEADING TO Coronary Artery Disease (CAD)
Caused by endothelial changes of increased oxidizing free radicals. Endothelium injured -> clotting buildup -> blood flow is turbulent -> flow changes creates small areas of stagnant blood (thrombus). Vessels become narrow from buildup.
Hypertension
Etiology:
Essential HTN has no known cause (think environmental factors, transient)
Secondary has a cause: obesity, DM, age (although more common now w/kids), inactivity, kidney disease
Mostly asymptomatic, unless extremes. Long-term heart, brain, kidney, eye, and artery complications. Left ventricular hypertrophy.
Stage 1 - 130-139/80-89
Stage 2 - >140-90
Stages of hypertension
Normal: <120/80
Elevated: 120-129/ <80
Stage 1: 130-139/80-89
Stage 2: >140/90
Orthostatic hypotension
Postural changes, and will eventually go away when baroreceptors sense the decrease and initiate peripheral constriction. -20 systolic, -10 diastolic
BP drops, HR rises
Cardiomyopathy
Can be hypertrophic, restrictive, or dilated -> compensates CO until it can’t
Clinical Manifestations/Signs & Symptoms:
Potentially nothing initially but can lead to dyspnea, SOB, reduced exercise intolerance, heart valve issues, abnormal cardiac rhythms, chest pain
Congenital Heart Defects
Etiology: preterm infants, teratogen exposure, genetics
(“left to right” example with septal defects)
Patent ductus arteriosus (PDA):
PDA doesn’t close so blood shunts from aorta into pulm artery and into lungs. Leads to HF and resp distress.
Atrial septal defect (ASD):
Opening in the septum b/t L&R atria. Blood shunts L to R and increases workload for RV. Leads to Afib, pulm HTN
Ventricular septal defects:
Opening in the septum b/t L&R ventricles. Asymptomatic, murmurs, CHF, tachy
Dysrhythmias/Arrhythmias
Impulse formation or impulse conduction issues
Normal Process: SA -> AV -> Bundle of His -> Purkinje fibers
Etiology: Hypoxia, electrolyte imbalances, cardiac surgery, structural changes in the heart, reduced coronary blood flow (MI), other medical comorbidities (thyroid disease, etc), congenital issues, antidysrhythmic drugs (cure them, but also cause them)
Sinus tachycardia
Supraventricular dysrhythmias (originate above ventricle)
- HR >100, normal w/exercise/meds/ETOH/caffeine, causes: Fever, Pain, Anemia, hypotension, pulmonary embolism, HF, Hyperthyroid, other medical conditions
Sinus bradycardia -
Supraventricular dysrhythmias (originate above ventricle)
HR <60, “sick sinus syndrome” - sinus node dysfunction or medications or hypothyroid, can be asymptomatic and normal in the 50s
Afib -
Supraventricular dysrhythmias (originate above ventricle)
most common, random atrial nodes firing randomly. Causes: hyperthyroid, sleep apnea, age, ETOH, meds. High risk of stroke.
(Aflutter, PAC)
V Tach -
Ventricular dysrhythmias (originate in ventricle)
Rapid, regular ventricular contractions, >100 that can cause reduced diastolic filling time; diminished cardiac output; Can degenerate into VFIB. Needs to be corrected if longer than 30 secs.
Torsades de Pointes -
Ventricular dysrhythmias (originate in ventricle)
Type of V tach w/ long QT time. Must be addressed immediately. **important when giving meds that can prolong QT.
V Fib -
Ventricular dysrhythmias (originate in ventricle)
Asynchronous ventricular contractions. Lose all CO and is life-threatening.
PVCs -
Ventricular dysrhythmias (originate in ventricle)
Ventricles are causing random and infrequent beats. Mainly benign, only concern when symptomatic or too many of them.
Conduction issues/heart blocks -
typically affect conduction to/from A/V node. Same etiologies.
First degree block
PR interval longer than normal
Second degree block
Type 1 “Wenckebach” - “PR” interval gradually increases until an A/V node conduction is missed
Type 2 - A/V conduction is randomly missed. More concerning than type 1; can require temporary / permanent pacing and can lead to complete heart block
Third degree block
Complete heart block. Atria and ventricles contracting separately - life threatening
Disease: Pericarditis
Etiology: viruses (most common), bacterial infection, MI, trauma, neoplasm, surgery, idiopathic
Pathophysiology
Disease Process: inflammation of the pericardium. There is local vasodilation with increased capillary permeability. This cases leaking of plasma proteins and accumulation of WBCs in the pericardial space
Clinical Manifestations/Signs & Symptoms: Triad of symptoms: Chest pain (worse with deep breathing or coughing), Pericardial friction rub, ECG changes (Sinus tachycardia, Diffuse ST elevation across all leads) Potentially a fever as well
Diagnosis: ECG. Chest x-ray, ECHO
Disease: Cardiac Tamponade
Diagnosed w/ Beck’s Triad: low blood pressure, distension of the jugular veins and decreased or muffled heart sounds on cardiac auscultation. EMERGENCY
Disease: Stenosis
Etiology: Valve gets thickened or hardened over time
Pathophysiology
Disease Process: Narrowing of the valve opening so it won’t open, Harder for blood to get through, Leads to hypertrophy of the cardiac muscle and increase in cardiac workload, decrease cardiac output
Aortic Valve Stenosis:
Blood backs up in LV (hypertrophy) and can reduce CO over time
Mitral Valve Stenosis:
Blood backs up in LA and can cause Afib, pulm HTN, pulm edema
Disease: Regurgitation
Etiology: Valve has been weakened or damaged
Patho
Disease Process: Inability of leaflets to adequately close, permits backward flow of blood when the valve should be closed. Results in a smaller percentage of oxygenated blood ultimately goes through the heart/lungs and back to the body as a result.
Aortic Valve Regurgitation:
Overload in the LV, leads to HF when heart can’t compensate anymore
Mitral Valve Regurgitation:
Backflow and overload in LA, leads to Afib
Tricuspid Valve Regurgitation:
Backflow and overload in RA, might be caused by failure and dilation of RV
Disease: Venous Diseases
Etiology: Circulation issues that can cause blood to pool or to damage valves
Disease Process: Blood trapped in the lower extremities because of poor circulation. Leads to valve insufficiency
Clinical Manifestations/Signs & Symptoms: Dependent edema, skin discoloration, ulcers
Diagnosis: D-dimers, ultrasounds, physical findings
Chronic venous insufficiency
Inadequate venous return over a long period caused by varicose veins or valvular incompetence. Edema and darker pigmentation from breakdown of RBCs. Causes ulcers. Venous HTN/stasis/hypoxia.
Venous thrombosis (DVT)
Blood clot in vein (typ. legs) due to poor circulation and stagnant blood that gives rise to platelet aggregation, d-dimer/US.
Varicose veins
Dilated, tortuous superficial veins from blood pooling from standing or venous pressure.
Disease: Heart Failure
Occurs when the heart cannot put out an adequate cardiac output for optimal circulatory perfusion. Plumbing - pump and pressures.
Etiology: Any structural or functional impairment of ventricular filling or ejection of blood.
Epidemiology: 1m new HF pts each year. 1 in every 33 Americans.
Left sided HF - LV dysfunction
can be sys or dias
Etiology: CAD, HTN, myocarditis, valve disease, tachycardiomyopathy
Clinical manifestations/S & S’s: Back up of blood into the pulm system - pulm HTN and edema/congestion. Systemic - perfusion issues (fatigue, AMS, oliguria, hypotension, decreased activity tolerance)
Right sided HF
Can also be sys or dias
Etiology: Left sided HF, pulm HTN, COPD, CAD, valve disease
Clinical manifestations/S & S’s: Back up of blood in the RA -> increased R pressure, backup into venous systemic circulation (hepatomegaly, splenomegaly, ascites, periph. edema, GI tract congestion)
LVEF calculations
end dias - end sys = SV
(SV/end dias) x 100 = LVEF (%)
HFrEF -
HF w/ reduced EF (LVEF ≤40%)
HFmrEF -
HF w/ mildly reduced EF LVEF (41%–49%)
HFpEF -
HF w/ preserved EF (LVEF ≥50%)
HF Compensatory Mechanisms
Initial -> Frank-Starling law
Sympathetic nervous system (detrimental long term)
RAAS (detrimental long term)
Both above are neurohormonal responses to cause vasoconstriction and sodium/fluid retention -> can lead to further HF
Natriuretic peptides - ANP & BNP produced by heart muscle stretch, fluid diuresed and vasodilation which (counteracts RAAS and positive long term
Frank-Starling law:
an increase in ventricular filling enhances the systolic performance of the heart and cardiac output, up to a point
Systolic HF
inability of the LV to pump blood, weakened heart muscle (dilated hypertrophy)
Diastolic HF
impaired ability of Vs to relax and fill, Vs become stiff
