Manifestation due to compensation
Tachycardia
Pallor
Oliguria (minimal urinary output)
– From decreased renal perfusion
– Renal failure is common and may require dialysis
Left and/or right-sided CHF
Left sided CHF Manifestations
Pulmonary congestion
Dyspnea
Orthopnea
Paroxysmal nocturnal dyspnea (PND)
Cough
– May be accompanied with hemoptysis (coughing blood)
Wheezes and rales audible on auscultation
Pleural effusion
Acute left sided failure will manifest with pulmonary edema
– Related to rapid accumulation of fluid and increased ventricular pressures
Right sided CHF Manifestations
Systemic congestion
Dependent edema
Digestive disturbances
Hepatomegaly / Splenomegaly
Distended jugular veins
Ascites (can get hernia)
Vascular disorders
Arterial disorders:
Hypertension
Aneurysm
Peripheral vascular disease
Venous disorders:
Thromboembolism (mainly DVT and PE)
Varicose veins
Hypertension
Consistent elevation of systemic arterial blood pressure
– Generally, BP >140/90 is considered mild hypertension for the average person
– For people with DM, BP > 130/80
– For those older than 80 years, BP >150/90
o Due to the stiffening of blood vessels that occurs naturally with aging 
Isolated systolic hypertension (ISH) is consistently
elevated SBP >140mmHg with diastolic (DBP) remaining within normal range (<90mmHg)
– ISH is rising within every age group and is strongly associated with increased risk of cardiovascular and cerebrovascular events
Types of Hypertension 
Primary hypertension (90%)
Also called essential or idiopathic
Most common type
– Gradual onset
– Most likely related to combination of aging and modifiable environmental and lifestyle factors
Secondary hypertension (10%)
Develops in response to other disease processes including:
– Renal disorders
o E.g. Glomerulonephritis, pyelonephritis, polycystic kidney
– Endocrine disorders
o E.g. Primary hyperaldosteronism, pheochromocytoma, Cushing’s syndrome, hyperthyroidism
– Vascular
o Renal artery stenosis
– Drug induced
o E.g. Steroids, estrogens
– Pregnancy
Note that many of the conditions related to the development of HTN are chronic in nature indicating a relationship between these processes and the chronic inflammation as well as physiologic/pathologic adaptations that occurs
Risk factors:
Nonmodifiable:
– Age
– Male gender
– Race
o E.g. African Americans have higher than average blood pressure
– Family history
o Genetic predisposition bis believed to be polygenic and related to defects associated with renal sodium excretion, SNS and RAAS activity, as well as cell membrane sodium and calcium transport
Modifiable
– Obesity
o Related to hormones secreted in obesity and insulin resistance that may develop
– High salt intake
o Leads to increased vascular volume from decreased salt excretion by the kidneys
– Physical activity
– Stress
– Smoking
– Alcohol consumption
– Drugs
o E.g. Oral contraceptives
Pathophysiology:
Sustained increase in peripheral resistance (arteriolar vasoconstriction), increase in blood volume, or both
– There is damage to the arterial wall leading to sclerosis (hardening and thickening) and narrowing of the arteries
– Weakening of the arterial wall can lead to an aneurysm
o Aneurysms are often asymptomatic and may go undetected
o Continued growth may lead to rupture and hemorrhage
– Decreased perfusion leads to organ ischemia and subsequent end-organ complications
Clinical manifestations:
Termed the silent killer as it is usually asymptomatic
– Diagnosis based on regular BP measurement
o Some may have physiologic/anatomic damage despite normal BP measurements
• If these changes remain undetected and untreated they may become established early in adulthood and begin accelerating in progression leading to increased risk for complications starting in middle decades of life
– Potential symptoms include:
o Morning occipital headache
o Manifestations of end organ failure
Clinical manifestations are usually related to tissue and/or organ damage outside of the vascular system and are therefore dependent on the system affected
These clinical manifestations include:
– Cardiovascular
o Liver hypertrophy
o Heart failure
o CAD
o PAD
– Cerebrovascular
o TIA
o Cerebral stroke
o Encephalopathy
– Visual System
o Retinopathy
o Papilledema
o Loss of vision
– Renal System
o Renovascular disease
o Renal failure
Resistant and Malignant Hypertension
Resistant HTN:
– Persistently elevated BP despite medical treatment
– Common risk factors: old age, obesity, renal disease
– Requires more aggressive control, often with 3 or more drugs
Malignant HTN:
– Rapidly progressive hypertension with DBP usually >140mmHg
– Hypertensive emergency
– Cerebral arterioles are unable to regulate blood flow to cerebral capillary beds leading to:
o Cerebral edema and cerebral dysfunction
o Papilledema
o Cardiac failure
o Uremia
o Retinopathy 
o Cerebrovascular accident (CVA; stroke)
– Severe HTN + acute target organ damage
Hypotension
BP < 90/60 and symptomatic
Causes:
Orthostatic hypotension
– Decreased BP upon standing
o Diagnostically, a decrease in SBP >20mmHg or decrease in DBP >10mmHg within 3 minutes of standing
– Due to lack of BP compensation in response to gravity
– Most common type of hypotension
Hypovolemia
Excessive vasodilation (usually peripherally)
Drug induced
Shock
– Hypotension is common and may require treatment with vasopressors to prevent complications from ischemia
Potential secondary disorders leading to hypotension include:
– Endocrine disorders
– Metabolic disorders
– Diseases of the central or peripheral nervous system
Manifestations
Dizziness
Blurred vision or vision loss
Syncope
Venous Thromboembolism (VTE)
Occlusion within venous bed by: clot (thrombus, embolus)
Pathophysiology:
Virchow triad (Vascular damage, Hypercoagulability, Circulatory stasis)
– Two key states of circulatory stasis are post-operative patients (especially orthopedic surgery) and atrial fibrillation
– Hypercoagulability
o Inherited abnormalities that increase risk in the absence of other usual risk factors include ATIII deficiency, prothrombin mutations, as well as deficiencies in proteins C, S
o Increased blood viscosity caused by eg. Polycythemia rubra vera
Main conditions associated with VTE:
– Deep vein thrombosis (DVT)
– Pulmonary embolism (PE)
Clinical manifestations DVT:
Swelling and pain in calf
Homan’s sign
– Lift the knee and dorsiflex foot elicits pain in affected extremity 
Clinical manifestations of PE:
– Dyspnea, chest pain on inspiration
– Tachycardia, cyanosis, hypotension
Diagnostic Findings:
Radiology
– Doppler Ultrasound for DVT
– CT and pulmonary angiography, V/Q scan for PE 
Laboratory Testing
– Elevated D-dimer
o Rule-out criteria
o A negative D-Dimer rules out PE, however, a positive D-Dimer does not confirm PE but instead indicates further testing
Varicose Veins
Distended and tortuous (twisted and turning) veins leading to pooling of blood
Pathophysiology
Valve damage caused by:
– Trauma to saphenous veins damaging one or more valves
– Gradual venous distention
o Caused by the action of gravity on blood in the legs while standing
o When a valve is damaged, a section of the vein is subject to increased pressure from a larger volume of blood leading to:
• Engorged vein
• Increased hydrostatic pressure and subsequent edema
Varicose Veins
Distended and tortuous (twisted and turning) veins leading to pooling of blood
Pathophysiology
Valve damage caused by:
– Trauma to saphenous veins damaging one or more valves
– Gradual venous distention
o Caused by the action of gravity on blood in the legs while standing
o When a valve is damaged, a section of the vein is subject to increased pressure from a larger volume of blood leading to:
• Engorged vein
• Increased hydrostatic pressure and subsequent edema
Risk factors:
▪ Age
▪ Female gender
▪ Family Hx
▪ Obesity
▪ Pregnancy
▪ DVT
▪ Prior leg injury